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Hepatic encephalopathy
Synonym(s): liver, brain
Introduction
- Syndrome caused by ammonia build up secondary to liver damage.
- Cause: severe hepatic insufficiency.
- Signs: signs may be intermittent, slowly progressive or acute from abnormal mentation, depression to ‘sudden’ death.
- Diagnosis: history and clinical signs suggestive; confirmation is by presence of laboratory findings indicative of liver failure.
- Treatment: supportive.
- Prognosis: very poor - hepatic damage is usually irreversible.
Presenting signs
- Early stage - depression and inappetance.
- Later stages - may see head pressing, visual impairment, circling; terminally generalized seizures or coma.
Age predisposition
- Any age.
- Some hepatic diseases have age predisposition and hence hepatic encephalopathy may be age related eg portosystemic shunt [Portosystemic shunt] occurs mostly in calves and fatty liver Fatty liver in mature cows.
Public health considerations
- Carcass condemnation in some cases but physiologically abnormal animals should not normally be entering the food chain.
Cost considerations
- Costs incurred with treatment and ultimate loss of the animal in most cases.
Special risks
- Compromised liver is less able to metabolize drugs.
- Compromised liver may not be producing sufficient clotting factors.
- Cattle may show altered behavior.
- Operator safety must be considered if animals shows increased aggression.
Pathogenesis
Etiology
- Poisoning Poisoning: investigation and treatment.
- Parasitism- fluke- Fasciola hepatica Fasciola hepatica.
- Fatty liver disease Ketosis/acetonemia and fatty liver
. - Portosystemic shunt.
- Endotoxemia causing hepatic damage eg due to mastitis/metritis.
- Other causes of liver damage.
Pathophysiology
- Hepatic encephalopathy is characterized by abnormal mentation due to protein, and other metabolites, crossing the blood-brain barrier during severe hepatic dysfunction and leading to diffuse cerebral impairment.
- The syndrome is incompletely understood.
- There are multiple theories, including:
- Systemic ammonia accumulation secondary to liver dysfunction occurs. Ammonia accumulates in the brain, acting as a neurotoxin.
- Alteration in amino acid metabolism due to liver dysfunction results in imbalance between aromatic amino acids (AAA) and branched chain amino acids (BCAA) AAA preferentially cross blood brain barrier and act as precursor for serotonin, an inhibitory neurotransmitter. End result is diffuse cerebral impairment.
- Hepatic dysfunction leads to systemic accumulation of metabolic byproducts, eg ammonia that causes an imbalance of fatty acids and excitatory and inhibitory neurotransmitters such as gamma amino butyric acid (GABA) or glutamate. These cross permeability-altered blood-brain barrier resulting in diffuse cerebral impairment.
Timecourse
- Variable- depends on underlying cause of hepatic disease.
Diagnosis
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Treatment
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Prevention
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Outcomes
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Further Reading
Publications
Refereed Papers
- Recent references from PubMed and VetMedResource.
- Masoud Davoudi S (2013) Study of Hepatic Problems in livestock. European Journal of Zoological Research 2 (4), 124-132.
- West H J (1997) Clinical and Pathological Studies in Cattle with Hepatic Disease. Vet Res Comms 21, 169–185 VetMedResource.
Other sources of information
- MSD Veterinary Manual.